The gene encoding catechol-O-methyltransferase (COMT), an enzyme which regulates prefrontal cortex dopamine, contains a common functional single nucleotide polymorphism (val158met, rs4680 G/A), which accounts for part of the interindividual variance in performance during working memory tasks and also predicts personality traits.

We examined the relationship between the val158met polymorphism and cognitive function as well as personality traits in 522 healthy individuals (mean age: 24.75 years, SD = 5.84, mean years of education: 15.59, SD = 2.65).

COMT val158met genotype was related in allele dosage fashion to performance in an executive function test, with the met/met carriers scoring highest. Subjects carrying the met/met genotype also scored higher in the disorganization domain of the SPQ-B personality inventory.

Consistent with evidence from previous studies, higher dopamine availability of the met/met genotype enhances prefrontally mediated executive function in healthy individuals.

Furthermore, we replicated findings from a recent study whereby the COMT genotype also predicts disorganized personality features.

We recently reported an association between TAAR6 (trace amine associated receptor 6 gene) variations and schizophrenia (SZ). We now report an association of a set of TAAR6 variations and clinical presentation and outcome in a sample of 240 SZ Korean patients. Patients were selected by a Structured Clinical Interview, DSM-IV Axis I disorders – Clinical Version (SCID-CV). Other psychiatric or neurologic disorders, as well as medical diseases, were exclusion criteria. To assess symptom severity, patients were administered the CGI scale and the PANSS at baseline and at the moment of discharge, 1 month later on average. TAAR6 variations rs6903874, rs7452939, rs8192625 and rs4305745 were investigated; rs6903874, rs7452939 and rs8192625 entered the statistical investigation after LD analysis. Rs8192625 G/G homozygosis was found to be significantly associated both with a worse clinical presentation at PANSS total and positive scores and with a shorter period of illness before hospitalization. No haplotype significant findings were found. The present study stands for a role of the TAAR6 in the clinical presentation of SZ. Moreover, our results show that this genetic effect may be counteracted by a correct treatment. Haplotype analysis was not informative in our sample, probably also because of the incomplete SNPs' coverage of the gene we performed. Further studies in this direction are warranted.

The clinical finding that depressive disorders are often associated with desynchronization of internal rhythms has encouraged the idea that resetting normal circadian rhythms may have antidepressant potential. Agomelatine, a naphthalene analog of melatonin, is both an agonist of human cloned melatonergic MT1 and MT2 receptors and a serotonin 5-HT2C receptor antagonist. Agomelatine combines zeitgeber (synchroniser of the circadian system) activity with neurotransmitter augmentation properties (enhances the levels of dopamine and noradrenaline in frontal cortex). The efficacy of agomelatine in treating depression has been shown in three short-term, pivotal, randomized, placebo–controlled studies. These studies have demonstrated agomelatine to be efficacious in Major Depressive Disorder at the standard dose of 25 mg/day, with the possibility of increasing doses to 50 mg/day in those patients with insufficient improvement. The number of adverse events during the treatment period was comparable to placebo. Four studies have shown the positive effect of agomelatine on sleep continuity and quality and shortening of sleep latency. Despite these promising data, further studies are needed to examine agomelatine's efficacy over a longer treatment period.

Depression has frequently been reported to be associated with other physical diseases and changes in the cytokine system. We aimed to investigate associations between a medical history of depression, its comorbidities and cytokine plasma levels in the Bavarian Nutrition Survey II (BVS II) study sample and in patients suffering from an acute depressive episode.

The BVS II is a representative study of the Bavarian population aged 13–80 years. The disease history of its 1050 participants was assessed through face-to-face interviews. A sub-sample of 568 subjects and 62 additional acutely depressed inpatients of the Max Planck Institute of Psychiatry participated in anthropometric measurements and blood sampling. Tumor necrosis factor-α (TNF-α) and soluble TNF receptor (sTNF-R) p55 and sTNF-R p75 plasma levels were measured using enzyme-linked immunosorbent assays.

A history of depression was associated with a higher incidence of high blood pressure, peptic ulcer, dyslipoproteinemia, osteoporosis, allergic skin rash, atopic eczema and thyroid disease.

Within the BVS II sample, participants with a history of depression differed from subjects who had never had depression with regard to sTNF-R p55 and sTNF-R p75 levels even when controlling for age, BMI and smoking status. Acutely depressed inpatients showed even higher levels of sTNF-R p55 and sTNF-R p75 than subjects in the normal population. TNF-α levels were also significantly elevated in acutely depressed patients.

These results confirm earlier studies regarding the comorbidities of depression and support the hypothesis that activation of the TNF-α system may contribute to the development of a depressive disorder.

Patients with affective disorders have often been reported to experience subjective changes in how they perceive the flow of time. Time reproduction tasks provide information about the memory component of time perception and are thought to remain unaffected by pulse rate disturbances in the pacemaker of the internal clock.

In our study, 30 patients with acute depression, 30 patients with acute mania, and 30 healthy subjects of all age groups were presented with a time reproduction task. Participants were asked to observe a stimulus presented on a computer screen for a certain length of time and, subsequently, to reproduce the stimulus for a similar length of time by pressing the space bar on the computer keyboard. Stimuli were presented to each subject for 1, 6, and 37 s.

On average, the time intervals reproduced by manic patients were shorter than those reproduced by depressed patients. Manic patients reproduced the short time interval (6 s) correctly, but under-reproduced the long time interval (37 s, P < 0.001). Depressed patients correctly reproduced the long time interval, but over-reproduced the short time interval (P < 0.001).

Remembering time intervals as having been longer than they actually were may lead to a slowed experience of time, as has been described in depressed patients; precisely the converse seems to apply to manic patients.

In the first third of the twentieth century, neuropathology seemed to offer the key to unlock the causes of psychiatric illness. Among the top centers devoted to the microscopic anatomy of the brain was that of Károly Schaffer in Budapest. Schaffer, a pioneer in the histopathology of Tay–Sachs–Schaffer disease, was also a charismatic teacher, bringing forth a school of investigators in psychopathology. Among them was László Meduna, who originated convulsive therapy. Despite the importance of the Schaffer school, it is almost unknown outside of Hungary, largely the result of the introduction of neurophysiological, neurochemical and molecular genetic methods that distracted attention away from histopathological contributions in psychiatry after the Second World War. The microscopic study of the brain and its diseases seemed increasingly less important.

The present biographical account of Károly Schaffer and his school seeks to bring this important story in the early history of biological psychiatry to a wider audience and explain why it has since been forgotten.

It is unknown whether a ‘jumping to conclusions’ (JTC) data-gathering bias is apparent in specific delusion sub-types. A group with persecutory delusions is compared with a sample of non-clinical controls on a probabilistic reasoning task. Results suggest JTC is apparent in individuals with the persecutory sub-type of delusions.

Rett syndrome is a genetically linked form of autism spectrum disorder (ASD) accompanied by intellectual disability (ID). The disorder is also characterized by cardiorespiratory dysregulation, disturbance in muscle tone, reduced brain growth and scoliosis. Over 300 studies have been published on the disorder, most of which has focused on identification of causative factors, which appears to be the result of mutations of gene MECP2. Rarely have adults with Rett syndrome been studied, and behavioral characteristics in these individuals are largely unknown. The present study aimed to extend what little is known about behavioral characteristics of Rett syndrome in adults, with particular emphasis on social, communicative, and adaptive behavior. Rett syndrome adults with severe ID were matched to autistic adults with ID and ID only controls. The implications of these data for more fully describing and diagnosing the condition in adults are discussed.